Abstract

Poultry consuming diets contaminated with citrinin excrete copious quantities of urine and exhibit increased water consumption. The present study was conducted to determine if citrinin acts directly on the kidneys and, if so, to provide a detailed physiological evaluation of the nephrotoxic effects of citrinin. Single Comb White Leghorn pullets were anesthetized and prepared for renal function studies. Ureteral urine was collected during a pre-infusion period (30 min), during unilateral renal portal infusion of 200 ppm citrinin (30 min), and during a recovery period following citrinin infusion (90 min). Pilot studies had shown that 200 ppm citrinin is the lowest dose capable of causing consistent unilateral responses when infused at a rate of .2 ml/kg body weight (BW)·min. The responses of the portal-infused kidneys were compared with the responses of the contralateral (uninfused) kidneys to determine the direct effects of citrinin.Citrinin had no acute direct (unilateral) effect on glomerular filtration rate, renal plasma flow rate, urine pH, or fractional calcium or magnesium excretion. Citrinin caused rapid unilateral increases in urine flow rates, free water clearance, and in fractional sodium, potassium, and inorganic phosphate excretion. Increased solute excretion did not compensate for increased free water clearance, as reflected by a significant decrease in urine osmolality. Recovery from the effects of citrinin occurred within 30 min after cessation of unilateral renal portal infusion. No histopathological damage was seen when citrinin was infused at 200 and 800 ppm, although dose-related increases in urine flow and decreases in urine osmolality were observed. These results indicate that citrinin acts directly on the kidneys to alter several tubular transport processes, and that the effects of citrinin are reversible.

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